Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA236101 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The goals of the microarray experiment were to determine the role of MAF1, the Toxoplasma gondii mediator of host mitochondrial association, on host cell gene expression by comparing infection of WT cells with Type II and Type II:MAF1 parasites. We also explored the role of MAF1 on host cell gene expression by comparing profiles of WT and MAVS KO MEFs infected with Type I and Type Imaf1KO parasites. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
2014-01-23 | GSE54285 | GEO
Project description:The goals of the microarray experiment were to determine the role of MAF1, the Toxoplasma gondii mediator of host mitochondrial association, on host cell gene expression by comparing infection of WT cells with Type II and Type II:MAF1 parasites. We also explored the role of MAF1 on host cell gene expression by comparing profiles of WT and MAVS KO MEFs infected with Type I and Type Imaf1KO parasites. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. WT MEFs were infected with Type II and Type II:MAF1 parasites at an MOI of 5. At 8 hpi RNA was harvested using TriZol. The Affymetrix IVT (16h) express kit was used for cDNA synthesis and labeling.
2014-01-23 | E-GEOD-54285 | biostudies-arrayexpress
Project description:The model is the second model of the publication "Modeling the role of lanthionine synthetase C-like 2 (LANCL2) in the modulation of immune responses to Helicobacter pylori infection" published in PlosOne by Leber, Bassaganya-Riera, Tubau-Juni, Zoccoli-Rodriguez, Viladomiu, Abedi, Lu, and Hontecillas.
Abstract:
Immune responses to Helicobacter pylori are orchestrated through complex balances of host-bacterial interactions, including inflammatory and regulatory immune responses across scales that can lead to the development of the gastric disease or the promotion of beneficial systemic effects. While inflammation in response to the bacterium has been reasonably characterized, the regulatory pathways that contribute to preventing inflammatory events during H. pylori infection are incompletely understood. To aid in this effort, we have generated a computational model incorporating recent developments in the understanding of H. pylori-host interactions. Sensitivity analysis of this model reveals that a regulatory macrophage population is critical in maintaining high H. pylori colonization without the generation of an inflammatory response. To address how this myeloid cell subset arises, we developed a second model describing an intracellular signaling network for the differentiation of macrophages. Modeling studies predicted that LANCL2 is a central regulator of inflammatory and effector pathways and its activation promotes regulatory responses characterized by IL-10 production while suppressing effector responses. The predicted impairment of regulatory macrophage differentiation by the loss of LANCL2 was simulated based on multiscale linkages between the tissue-level gastric mucosa and the intracellular models. The simulated deletion of LANCL2 resulted in a greater clearance of H. pylori, but also greater IFNγ responses and damage to the epithelium. The model predictions were validated within a mouse model of H. pylori colonization in wild-type (WT), LANCL2 whole body KO and myeloid-specific LANCL2-/- (LANCL2Myeloid) mice, which displayed similar decreases in H. pylori burden, CX3CR1+ IL-10-producing macrophages, and type 1 regulatory (Tr1) T cells. This study shows the importance of LANCL2 in the induction of regulatory responses in macrophages and T cells during H. pylori infection.
2016-12-01 | MODEL1611160001 | BioModels
Project description:The model is first model of tissue level cellular immune responses to H. pylori in the publication, "Modeling the role of lanthionine synthetase C-like 2 (LANCL2) in the modulation of immune responses to Helicobacter pylori infection" in PlosOne by Leber, Bassaganya-Riera, Tubau-Juni, Zoccoli-Rodriguez, Viladomiu, Abedi, Lu, and Hontecillas.
Abstract:
Immune responses to Helicobacter pylori are orchestrated through complex balances of host-bacterial interactions, including inflammatory and regulatory immune responses across scales that can lead to the development of the gastric disease or the promotion of beneficial systemic effects. While inflammation in response to the bacterium has been reasonably characterized, the regulatory pathways that contribute to preventing inflammatory events during H. pylori infection are incompletely understood. To aid in this effort, we have generated a computational model incorporating recent developments in the understanding of H. pylori-host interactions. Sensitivity analysis of this model reveals that a regulatory macrophage population is critical in maintaining high H. pylori colonization without the generation of an inflammatory response. To address how this myeloid cell subset arises, we developed a second model describing an intracellular signaling network for the differentiation of macrophages. Modeling studies predicted that LANCL2 is a central regulator of inflammatory and effector pathways and its activation promotes regulatory responses characterized by IL-10 production while suppressing effector responses. The predicted impairment of regulatory macrophage differentiation by the loss of LANCL2 was simulated based on multiscale linkages between the tissue-level gastric mucosa and the intracellular models. The simulated deletion of LANCL2 resulted in a greater clearance of H. pylori, but also greater IFNγ responses and damage to the epithelium. The model predictions were validated within a mouse model of H. pylori colonization in wild-type (WT), LANCL2 whole body KO and myeloid-specific LANCL2-/- (LANCL2Myeloid) mice, which displayed similar decreases in H. pylori burden, CX3CR1+ IL-10-producing macrophages, and type 1 regulatory (Tr1) T cells. This study shows the importance of LANCL2 in the induction of regulatory responses in macrophages and T cells during H. pylori infection.
2016-12-01 | MODEL1611160002 | BioModels
Project description:Purpose: To understand the role of SUMOylation of c-Fos in the differential regulation of target genes and altered cellular pathways upon STm infection. To address this, we performed a RNA-seq experiment with stable over expressing WT-FOS or SUMO-def-FOS in f10 c-FOS-Knock out MEFs upon STm infection. Methods: Three biological replicates of c-FOS-KO-WT-FOS, c-FOS-KO-WT-FOS with salmonella infection, c-FOS-KO-SUMO-def-FOS and c-FOS-KO-SUMO-def-FOS with salmonella infection, cells were collected and total RNA was extracted according to kit's protocol. The total RNA was used to generate a cDNA library using Quantseq 3' mRNA kit. Results: Transcriptional profiling revealed that genes involved in immune response, proliferation, metastasis etc. are differentially regulated in salmonella infected c-FOS-KO-SUMO-def-FOS MEFs compare to salmonella infected c-FOS-KO-WT-FOS MEFs. Conclusions: Our study revealed the extensive transcriptomics analysis from c-FOS-KO-WT-FOS and c-FOS-KO-SUMO-def-FOS MEFs upon salmonella infection. We found that SUMOylation of c-Fos provides selectivity that causes differential regulation of target genes which are involved in immune response, proliferation etc. pathways of host. Together, our findings illuminate an important regulatory role played by SUMOylated c-Fos upon STm infection.
2022-05-08 | GSE201782 | GEO
Project description:mRNA profiles of beta-actin knockout (KO) and wild-type (WT) MEFs induced to adipocyte-like feature to study how global transcriptome changes during differentiation
2019-05-07 | GSE130765 | GEO
Project description:The expression of interferon-related genes was more enhanced in irradiated ATM-deficient mouse embryonic fibroblasts (MEFs) than in irradiated ATM wild-type MEFs. Nonirradiated-ATM-WT vs Irradiated-ATM-WT vs Nonirradaited-ATM-KO vs IrradiatedATM-KO
2012-06-19 | E-GEOD-23116 | biostudies-arrayexpress
Project description:Myeloid dendritic cells from WT, Irf3-/-xIrf7-/-, Irf3-/-xIrf5-/-xIrf7-/-, Mavs-/- (IPS1-/-)and Ifnar-/- mice were infected with West Nile virus to assess the contributions of specific signaling and transcription factors in initiating the antiviral response RPMI + rmGM-CSF purified bone marrow derived myeloid DC (mDC), mock and WNV infected with insect derived virus and RNA isolated at 24 hours post infection . Each genotype has matched mock and infected samples. n=6 for WT mock, WT infected, IFNAR mock, IFNAR infected, IRF3x7 infected; n=5 IRF3x7 infected; n=3 IRF3x5x7 mock, IRF3x5x7 infected, MAVS mock, MAVS infected. RNA was prepared using the Illumina bead station assay and hybridized to Illumina RefSeq-8 V2 BeadChips. Note: MAVS=IPS1
2013-04-23 | E-GEOD-41355 | biostudies-arrayexpress
Project description:Using a supercritical fluid chromatography-mass spectrometry (SFC-MS)-based methodology, we quantified phosphoinositides (PIPs) species in mouse embryonic fibroblasts (MEFs) from WT or FIP200 KO mice during autophagosome formation.
2021-06-02 | ST001818 | MetabolomicsWorkbench
Project description:This project looks at the effect a chemical modulator targeting PI3Kα has on the phosphoproteome of PI3Kα-WT and PI3Kα-KO MEFs. PI3K signalling is a critical regulator of numerous cellular processes such as proliferation, apoptosis, migration, invasion, metabolism, cell growth and autophagy. The PI3K pathway is frequently hyperactivated in cancer, commonly due to activating mutations or via loss of the lipid phosphatases that negatively regulate the pathway. We have recently identified a new small molecule modulator of the PI3K pathway and have used an unbiased phosphoproteomics approach to examine the impact of this compound on signalling pathways in cells that are wild-type and knockout for PI3K. Immortalised mouse embryonic fibroblasts (MEFs) isolated from PI3Kα-WT and PI3Kα-KO embryos were treated with and without the modulator (5 µM), exploring early (15 min) and late (4 h) time points. Insulin is a well-characterised activator of PI3K. Therefore, PI3Kα-WT MEFs were also treated with insulin (100 nM) as a positive control to compare with the PI3K modulator.
2023-03-06 | PXD027993 | Pride